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Related Experiment Videos

Differences in steady-state inactivation between Na channel isoforms affect local anesthetic binding affinity

S N Wright1, S Y Wang, R G Kallen

  • 1Department of Anesthesia Research Laboratories, Harvard Medical School, Boston, Massachusetts, USA. swright@zeus.bwh.harvard.edu

Biophysical Journal
|August 1, 1997
PubMed
Summary

Local anesthetics like cocaine and lidocaine affect cardiac and skeletal muscle sodium channels similarly. Cardiac sodium channels are more sensitive due to a higher proportion being in a high-affinity inactivated state at physiological potentials.

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Area of Science:

  • Pharmacology
  • Cardiovascular Physiology
  • Neuroscience

Background:

  • Cocaine and lidocaine are local anesthetics (LAs) that block sodium (Na) currents.
  • Cocaine is cardiotoxic, inducing arrhythmia, while lidocaine is an antiarrhythmic.
  • LAs have clinically relevant effects at non-obvious concentrations on nerve and skeletal muscle.

Purpose of the Study:

  • Compare cocaine and lidocaine affinities for human cardiac (hH1) and rat skeletal (mu 1) muscle Na channels.
  • Investigate the basis for differential sensitivity of cardiac tissue to these LAs.

Main Methods:

  • Transiently expressed hH1 and mu 1 Na channels in HEK 293t cells.
  • Measured cocaine and lidocaine affinities for resting and inactivated channel states.

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Main Results:

  • Resting and inactivated channel affinities for cocaine and lidocaine were similar between hH1 and mu 1 channels.
  • Cardiac hH1 channels showed a higher percentage in the inactivated state at physiological resting potentials (-100 to -90 mV).

Conclusions:

  • Greater cardiac sensitivity to cocaine and lidocaine is not due to higher LA receptor affinity.
  • The increased sensitivity results from a larger proportion of cardiac Na channels being in the high-affinity inactivated state at physiological potentials.